A 17 years old male presented with recurrent palpitations, vertigo and the feeling of pulsations in the neck over the past 6 months. On first examination the 12-Lead ECG was unremarkable, physical did not reveal any pathologies. Neither did the echocardiogram.
During hospital stay the monitoring ECG revealed the following:
The first 3 beats are Sinusbeats with constant PR interval. The fourth beat has no previous P wave. Beats 5 & 6 are Sinus again. Now, the 7th beat, a premature atrial contraction (PAC) appears. Ultimately following this beat is another PAC which shows as a P wave at the end of the T wave (figure below: blue arrow) of the prior PAC. Then a long A-V conduction takes place between the P wave and the next QRS complex. This is due to A-V jump (or rather A-His jump; figure below: orange line), when the conduction from the atrium "jumps" from the fast pathway (which is rendered refractor by the prior PAC) to the slow pathway entering the AV node.
As you know, dual AV nodal physiology (i.e. the presence of a slow and a fast pathway leading towards the AV node) is mandatory for the initiation of AVNRT. This dual AV nodal physiology is what you see in the 3rd beat (figure below: orange line). It is the same A-V jump that you encountered at tachycardia initiation. The first QRS complex is conducted via the fast pathway, the consecutive QRS is conducted from the same atrial activation via the slow pathway through the AV node.
The tachycardia that starts with PAC and A-V jump then shows narrow complex, regular tachycardia with P in the S wave (close look reveals blunted spike of the S wave, as compared to the regular sinus beats in lead II (R-P interval <70ms). This is typical of AVNRT.
Additionally, reentry tachycardias often terminate by PACs. This is what happened later in the tracing:
The 9th beat is a PAC (P wave negative in lead II and prior to QRS) which terminates tachycardia. The subsequent beat (10th beat) is already sinus again.